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Influence of Kamijihwang-hwan on the Hypoxic Damage of Cultured Cerebral Neurons from mouse and SK-N-MC cells  

Kyung Baek Yeun (Department of Pathology, College of Oriental Medicine, Wonkwang University)
Ju Sung Min (Department of Pathology, College of Oriental Medicine, Wonkwang University)
Kim Kun Jun (Department of Pathology, College of Oriental Medicine, Wonkwang University)
Kim Dae Keun (Department of Pathology, College of Oriental Medicine, Wonkwang University)
Kang Jeong Ho (Department of Pathology, College of Oriental Medicine, Wonkwang University)
Lee Young Chan (Department of Pathology, College of Oriental Medicine, Wonkwang University)
Lee Jun (Department of Pathology, College of Oriental Medicine, Wonkwang University)
Kim Young Mok (Department of Pathology, College of Oriental Medicine, Wonkwang University)
Jeon Byung Hun (Department of Pathology, College of Oriental Medicine, Wonkwang University)
Publication Information
Journal of Physiology & Pathology in Korean Medicine / v.17, no.4, 2003 , pp. 1082-1091 More about this Journal
Abstract
To elucidate the neuroprotective effect of Kamijihwang-hwan(KSH) on nerve cells damaged by hypoxia, the cytotoxic effects of exposure to hypoxia were determined by XTT, NR, MTT and SRB asssay. The activity of catalase and SOD was measured by spectrophometry, and TNF-α and PKC activity was measured after exposure to hypoxia and treatment of Kamijihwang-hwan(KSH) water extract(KJHWE). Also the neuroprotective effect of KJHWE was researched for the elucidation of neuroprotective mechanism. The results were as follows ; Hypoxia decreased cell viability measured by XTT, NR assay when cultured cerebral neurons were exposed to 95% N2/5% CO₂ for 2～26 minutes in these cultures and KJHWE inhibited the decrease of cell viability. H₂O₂ treatment decreased cell viability measured by MTT, and SRB assay when cultured cerebral neurons were exposed to 1-80 uM for 6 hours, but KJHWE inhibited the decrease of cell viability. Hypoxia decreased catalase and SOD activity, and also TNF-α and PKC activity in these cultured cerebral neurons, but KJHWE inhibited the decrease of the catalase and SOD activity in these cultures. Hypoxia triggered the apoptosis via caspase activation and internucleosomal DNA fragmentation. Also hypoxia stimulate the release of cytochrome c form mitochondria. KJHWE inhibited the apoptosis via caspase activation induced by hypoxia. From these results, it can be suggested that brain ischemia model induced hypoxia showed neurotoxity on cultured mouse cerebral neurons, and the KJHWE has the neuroprotective effect in blocking the neurotoxity induced by hypoxia in cultured mouse cerebral neurons.
Keywords
Kamijihwang-hwan(加味地黃丸); hypoxia; cerebral neuron; SK-N-MC;
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